Two phases of caloric restriction

As regards muscle mass retention, caloric restriction appears to function in two separate ways depending on the severity and duration of the caloric deficit. With a small deficit, the effect of caloric restriction is to reduce muscle protein synthesis (MPS) rates. With a large deficit, the effect of caloric restriction is to increase muscle protein breakdown (MPB) rates by behaving like a stressor.

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#1. Caloric restriction can cause muscle atrophy by reducing basal MPS rates

Caloric restriction of any magnitude and duration causes atrophy by reducing basal MPS rates. This accelerates muscle atrophy between workouts and reduces the beneficial effect of workouts (read more).

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#2. Caloric restriction can cause muscle atrophy by increasing muscle protein breakdown rates

Elevated cortisol levels cause atrophy by increasing basal muscle protein breakdown (MPB) rates. This can occur as a result of sleep deprivation or traumatic injury but there are also a number of experimental models involving exogenous glucocorticoids (read more).

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While a suppression of MPS rates is the most commonly-reported feature of caloric restriction, some studies have reported an initial reduction in MPB rates (which would be expected given the accompanying reduction in MPS rates) before a subsequent increase in MPB rates when the magnitude of the calorie deficit is relatively high.

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#3. Severe caloric restriction elevates glucocorticoid levels and produces oxidative stress

Severe caloric deficits increase circulating endogenous levels of glucocorticoids (while mild caloric deficits do not). This suggests that there is a shift in the effect of caloric restriction according to the magnitude of the deficit.

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Interestingly, in human studies measuring lean body mass losses during caloric restriction, there is a shift from maintenance of lean body mass to loss of lean body mass at a deficit of approximately 500 kcal per day. Assuming a typical caloric intake of 2,500 kcal/day, that would represent a deficit of approximately 20% of habitual calorie intake, which lines up quit4e well with the inflection point in the animal models.

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#4. Severe caloric restriction reduce muscle sensitivity to dietary protein levels

Severe caloric deficits also reduce the sensitivity of muscle fibers to the availability of amino acids that support hypertrophy, while does not seem to be a problem during mild caloric deficits. Lean mass is not spared during periods of severe caloric restriction irrespective of the proportion of the diet comprised of protein, apparently due to the suppression of signaling in the mTOR pathway. Feasibly, this might also be related to the actions of the circulating glucocorticoids.

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The exact same phenomenon has been observed in controlled rodent models. As in human trials, the protein content of a diet does not affect the resulting muscle atrophy experienced nor the reduction in the anabolic signals that govern muscle protein synthesis.

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Conclusions

Caloric restriction appears to cause muscle atrophy in two separate ways depending on the size of the deficit. During small deficits, caloric restriction primarily reduces muscle protein synthesis (MPS) rates. This problem can be addressed by intelligent programming, as can be seen from the absence of lean mass loss in studies examining small calorie deficits in combination with strength training. During larger deficits, caloric restriction behaves like a stressor and increases muscle protein breakdown (MPB) rates. Indeed, when measuring the effects of severe caloric restriction in animal models, the magnitude of the calorie deficit is closely related to the size of the stress hormone response. Small deficits do not cause an increase in circulating glucocorticoid levels, while large deficits increase glucocorticoid production dose-responsively. Also, during animal models of fasting, there is initially a reduction in both MPS and MPB rates. However, as the deficit persists and generates a stress response, MPB rates increase dramatically. Increases in MPB rates are known to be caused by glucocorticoid production. Glucocorticoids cause muscle atrophy by stimulating an increase in oxidative stress within muscle fibers, causing elevations in MPB rates to deal with the damaged proteins and leading to net negative protein balance. Bodybuilders should avoid severe caloric deficits in order to maintain muscle mass while dieting.